Impact of Aortic Diameter Measurements at Three Anatomical Landmarks on Left Ventricular Output Calculation in Neonates

2021 ◽  
Author(s):  
Benjamim Ficial ◽  
Elena Bonafiglia ◽  
Antonella Gangemi ◽  
Maria Clemente ◽  
Alessia Cappelleri ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Aortic Diameter ◽  
Anatomical Landmarks ◽  
Left Ventricular Output

scholarly journals Erratum to: Perfusion index and left ventricular output correlation in healthy term infants

2017 ◽  
Vol 176 (8) ◽  
pp. 1019-1019
Author(s):  
Iuri Corsini ◽  
Alessandra Cecchi ◽  
Caterina Coviello ◽  
Carlo Dani
Keyword(s):  
Left Ventricular ◽  
Perfusion Index ◽  
Term Infants ◽  
Left Ventricular Output

In Reply: Cerebral Blood Flow

PEDIATRICS ◽  
1982 ◽  
Vol 70 (6) ◽  
pp. 1013-1014
Author(s):  
RAUL BEJAR
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Gastrointestinal Tract ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Left Ventricular Output ◽  
Patent Ductus

Baylen and Emmanouilides give the impression that their abstract was misquoted in our commentary. We would like to explain our interpretation of their data. In the abstract, Baylen et al indicate that they measured regional blood flows (RBF) in premature fetal lambs, expressing them as a percentage of the left ventricular output (LVO) before and after patent ductus arteriosus (PDA) closure. Their results (percent of LVO) before and after PDA closure were: lung, 42.7% vs 8.4% (P < .01); carcass, 35% vs 55% (P < .01); heart, 5.5% vs 10.2% (P < .05); gastrointestinal tract, 5.1% vs 9.3% (P < .05); brain, 2.7% vs 3.4% (P = NS); kidney, 2.2% vs 3.3% (P = NS); liver, 3.2% vs 5.7% (P = NS).

Abstract 308: Cardiac Cycle Affects Ultrasound Measurements of Ascending Aortic Diameter in a Marfan Mouse Model

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Zheying Chen ◽  
Hisashi Sawada ◽  
Debra Rateri ◽  
Alan Daugherty ◽  
Mary Sheppard
Keyword(s):  
Cardiac Cycle ◽  
Interobserver Variability ◽  
Innominate Artery ◽  
Aortic Diameter ◽  
Ultrasound Images ◽  
Anatomical Landmarks ◽  
Wild Type ◽  
Ultrasound Measurements ◽  
Fibrillin 1 ◽  
Ascending Aortic Diameter

Objective: Ultrasound measurements of aortic diameter are a common endpoint in preclinical studies. However, there is a lack of standardization in both image capture and analysis. For our study, we developed a standardized protocol for measuring ascending aortic diameter and examined effects of cardiac cycle in wild type and fibrillin-1 hypomorphic (FBN mgR/mgR ) mice. Methods and Results: Twelve week old male and female FBN mgR/mgR mice were anesthetized and maintained at a heart rate of 450-550 beats per minute. Ultrasound images were captured using a Vevo 2100 system with a 40MHz tranducer. Images captured were standardized according to two anatomical landmarks: the innominate artery branchpoint and aortic valves. The largest luminal ascending aortic diameter between the sinotubular junction and the innominate artery were measured in mid-systole and end-diastole by two blinded, independent observers. Aortic diameters were significantly different (p<0.05) when comparing systole and diastole within gender and genotype. Interestingly, wild-type male (n=4) and female (n=3) mice exhibited a 19% and 15% expansion of the ascending aorta respectively during systole compared to diastole. This difference was not recapitulated in either male (n=6) or female (n=5) FBN mgR/mgR mice (4% expansion in both; p<0.05 vs wild-type). Agreement between observers was excellent (R^2 = 0.99) but interobserver variability was a mean of .09 mm (%CV = 5%) Conclusion: As expected, there is a difference in aortic diameters between wild-type and FBN mgR/mgR mice. Luminal aortic diameters in FBN mgR/mgR vs wild-type mice of both genders are affected by cardiac cycle. Mid-systolic aortic expansion in wild-type vs FBN mgR/mgR mice were different. Error introduced by interobserver variability impacts ascending aortic measurements. Altogether, these phenomena may confound analyses of aortic dilation in FBN mgR/mgR mice, especially when studying interventions with modest effect sizes.

Measurement of Left Ventricular Output

1954 ◽  
Vol 7 (3) ◽  
pp. 258-270 ◽  
Author(s):  
Lysle H. Peterson ◽  
Martin Helrich ◽  
Leon Greene ◽  
Carolyn Taylor ◽  
Gaston Choquette
Keyword(s):  
Left Ventricular ◽  
Left Ventricular Output

Radionuclide Assessment of the Natural Heart Ejection Fraction before and after LVAD Implantation

1989 ◽  
Vol 12 (1) ◽  
pp. 41-46 ◽  
Author(s):  
A. Moritz ◽  
C. A. Napoli ◽  
D. Feiglin ◽  
N. Uchida ◽  
H. Harasaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Cleveland Clinic ◽  
Blood Pool ◽  
Left Ventricular ◽  
Before And After ◽  
Movement Artifacts ◽  
Holstein Calves ◽  
Left Ventricular Output ◽  
The Individual

Complete pressure unloading of the ventricles can preserve ischemically damaged myocardium. Most clinical left heart assist device (LVAD) systems used after ischemic injury of the heart apply atrial cannulation which does not ensure pressure unloading. In order to assess the effect of the implantation of an intracorporeal LVAD on the function of the natural heart, we determined the ejection fraction (EF) in four male Holstein calves (90–105 kg) before and after insertion of a Cleveland Clinic pneumatic LVAD. A gated blood pool scan was obtained with a gamma camera after injection of 40 mCi Tc-labelled albumin. The animals were restrained in a sling to avoid movement artifacts. All animals showed a drop of 65 ± 12% to 42 ± 14% EF in the first postoperative (p.o.) week. Left ventricular output did not maintain sufficient blood pressure as assessed by pump-off tests. Systolic blood pressure dropped from 122 ±6.5 mm Hg to 81 ± 6 mm Hg without pump support on the morning of the first p.o. day. Apical coring and possible restrained heart movement by the implanted LVAD may lead to impaired myocardial function that renders the individual LVAD dependent until adaptative corrections take place.

Agreement of Cardiac Output Measurements between Bioreactance and Transthoracic Echocardiography in Preterm Infants during the Transitional Phase: A Single-Centre, Prospective Study

Neonatology ◽  
2020 ◽  
Vol 117 (3) ◽  
pp. 271-278 ◽  
Author(s):  
Lizelle Van Wyk ◽  
Johan Smith ◽  
John Lawrenson ◽  
Willem Pieter de Boode
Keyword(s):  
Cardiac Output ◽  
Preterm Infants ◽  
Transthoracic Echocardiography ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Percentage Error ◽  
Preterm Neonates ◽  
Non Invasive ◽  
Left Ventricular Output ◽  
Transitional Phase

<b><i>Introduction:</i></b> Bioreactance cardiac output (CO) monitors are able to non-invasively and continuously monitor CO. However, as a novel tool to measure CO, it must be proven to be accurate and precise. <b><i>Objective:</i></b> To determine the agreement between CO measured with a bioreactance monitor and transthoracic echocardiography-derived left ventricular output parameters in preterm infants. <b><i>Methods:</i></b> This is a prospective observational study in 63 preterm neonates with non-invasive respiratory support, not requiring inotrope support. The infants underwent continuous bioreactance monitoring of CO and stroke volume (SV) and simultaneous transthoracic echocardiography every 6 h until 72 h of life. <b><i>Results:</i></b> The agreement between bioreactance and transthoracic echocardiography, for both SV and CO, was poor. The percentage error was 67.5% for SV and 71.6% for CO. The mean error was 60.4% for SV and 69.8% for CO. Bias was affected by numerous variables. After correcting for time, CO and SV bias were significantly affected by the presence of an open patent ductus arteriosus and the level of CO. <b><i>Conclusion:</i></b> Bioreactance cannot be considered interchangeable with transthoracic echocardiography to measure CO in preterm infants during the transition phase. Agreement between bioreactance and other CO metrics should be assessed before concluding its accuracy or inaccuracy in neonates.

Prostaglandins and fetal cardiac output distribution in the lamb

1985 ◽  
Vol 248 (6) ◽  
pp. H853-H858
Author(s):  
E. B. Sideris ◽  
K. Yokochi ◽  
F. Coceani ◽  
P. M. Olley
Keyword(s):  
Cardiac Output ◽  
Right Ventricular ◽  
Main Pulmonary Artery ◽  
Left Ventricular ◽  
Base Line ◽  
Pulmonary Flow ◽  
Pulmonary Vasodilator ◽  
Distribution Right ◽  
Output Ratio ◽  
Left Ventricular Output

With the use of a triple thermodilution technique in 17 fetal lambs, combined with microsphere estimations in 7, the effects of indomethacin prostaglandin (PG) I2 and PGE2 on cardiac output and its distribution were measured. Indomethacin (0.2 mg/kg) induced a main pulmonary artery-to-aorta pressure gradient, which peaked within 45–60 min and persisted for 2–3 h. PGE2 abolished this gradient (threshold 50 ng X kg-1 X min-1), while PGI2 in doses up to 100 ng X kg-1 X min-1 increased it. Indomethacin did not change total cardiac output but altered its distribution (right ventricular output, left ventricular output) and increased the percentage of right ventricular output flowing to the lungs. Ductal flow decreased concomitantly. After indomethacin, PGI2 further decreased ductal flow, increased pulmonary flow, and decreased pulmonary vascular resistance. PGE2 restored the original right ventricular-to-total cardiac output ratio, although ductus flow did not return to base-line levels. Pulmonary resistance increased slightly, reflecting decreased pulmonary flow, associated with decreased right ventricular output. Thus PGE2 was more effective on the ductus than on the pulmonary circulation. PGI2 did not relax the ductus but was a potent pulmonary vasodilator. Neither PGI2 nor PGE2 nor indomethacin changed total cardiac output but all altered its distribution.

scholarly journals The effects of increasing mean arterial pressure on left ventricular output in newborn lambs.

1990 ◽  
Vol 67 (1) ◽  
pp. 78-83 ◽  
Author(s):  
G F Van Hare ◽  
J A Hawkins ◽  
K G Schmidt ◽  
A M Rudolph
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Left Ventricular Output
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